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PHSI 208 > GIT 2 > Flashcards

GIT 2 Flashcards

1
Q

describe small int motility in addition to peristalsis?

A
  1. Segmentation contractions
    –chyme moves back and forth, mixes with bicarb (to neutralize acid) and enzymes for digestion
    –initiated by ICCs
    –increased by Distension, gastrin (anrtal G cells), extrinsic nerve activity (parasymp)
  2. MMC
    • Start when most meal absorbed
      • Release of sm. intestinal hormone motilin - Strong repetitive peristaltic waves
      • From the stomach to end of small
        intestine
      • “Sweep” remaining contents towards the
        large intestine (colon)
        “house keeping” role—cleans out gut of indigestible “food”— e.g. someone accidentaly swallows a ring, etc-> eventually is passed because of the MMC
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2
Q

when does MMC start in small int?

A

when does MMC start? when fasting— no food in stomach or small int; motilin is elevated during fasting—> causes the contractions
—also ghrelin is also increased—tells individual to go and find food

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3
Q

secretin is released in response to the acid
CCK—released in response to lipids
—both slow down gastric emptying

A

ya

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4
Q

what are the hormones released in small int, and what are their functions?

A 
GI Hormones: (all peptides)
Gastrin--small peptides
CCK (cholecystokinin) --fats
Secretin--acid
GIP (gastric inhibitory peptide)--fat and glucose 
Motilin--fasting
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5
Q

other secetions of small int

A

mucus and water
lysozyme
no digestive enzymes secretion, but does contain brush border enzyme enterokinase

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6
Q

describe the exocrine funtions the pancreas (what it secretes, and what stims it)

A

secretes mucus, water, enzymes, directly into duodenum–stim’d by presence of digestive juices

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7
Q

secretions in GI can be influced by parasymp and symp innveration (MyP and submucosa plexous) but also hormonal–e.g. CCK and secretin influence secretion

A

ya

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8
Q

what are the pancreatic enzymes?

A 
Released by acinar cells--under stim of CCK and secretin?
Trypsinogen* 
Chymotrypsinogen* 
Proelastase* 
Procarboxypeptidase A* and B*
Procolipase*
Pancreatic lipase
Bile salts activated lipase 
Cholesteryl ester hydrolase Prophospholipase A2*
Pancreatic alpha-amylase
Ribonuclease Deoxyribonuclease
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9
Q

what are ductular cells and what do they release?

A

cells that line the ductules of the pancreas; secrete ions, water, and bicarb
Cations: Na, K, Ca, Mg
Anions: HCO3, Cl, SO42-, HPO42-

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10
Q

what is pancreatitis?

A

disease where proteases are already active in pancreas–start digesting and damaging pancreas

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11
Q

describe protein activation in the small int (duodenum)

A

pancreatic juice (high in acid) activates enterokinase on the APICAL membrane; enterokinase cleaves trypsinogen to trypsin; trypsin then activates all other pancreatic proteases (trypsin is the “master switch”)

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12
Q

CCK causes pancreatic enzyme and bicarbonate secretion.

Secretin is a potent stimulus for pancreatic and bile bicarbonate secretion.

A

ya

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13
Q

how does CCK facilitate lipid degradation?

A

contracts gall bladder–bile empties into duodenum (acts on pancreas too–bicarb release)
–also acts on acinar cells to release digestive enzymes

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14
Q

role of sphinc of Oddi?

A

sphincter of Oddi—controls amount of liver (biliary) and pancreatic secretins; most secretions of liver are stored and conc’d in the gallbladder;

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15
Q

what is the purpose of bile acids, and how are they created?

A

secreted from the liver/gal bladder; required for lipid digestion; primary bile acid is released from the liver and conc’d in the gall bladder until needed; it is conjugated with taurine/glycine;
secondary bile acids occur from colonic bacteria enzymes–deconjugated and remove the OH; goes back to the liver for recycling via enterohepatic circulation;

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16
Q

what are gallstones, and how do they form?

A

two types: Ca bilirubinates and cholesterol stones–too much chol ppts;

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17
Q

what factors promote gall stone formation?

A

bile stasis–bile stasis—bile remains in gall bladder bc you are skipping meals or meals low in fat—>gall does not need to squeeze out biles
chol supersaturation in bile–liver tries to excrete excess cholesterol into the bile
—cholesterol can remain in gall bladder and it concentrates the liver secretions, get gall bladder stones
nucleation factors–bacteria get into gall bladder; attracts chol and ppts

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18
Q

symptoms of gall stones?

A

pain below right scapula after eating fatty meal

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19
Q

regulations

A

– Fatty acids and proteins in the duodenum cause release of
CCK (cholecystokinin)
– CCK increases gallbladder contraction
– Production of bile is increased by stimulation of the vagus nerves and by the hormone secretin

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20
Q

what are the types of cells found on the villi, and what can they be separated into?

A

villi cells–microvilli; mostly absorb nutrients
crypt cells–mostly secrete (e.g. water, bile, salts);
–goblet cell, secretes mucus
–enteroendocrine cell–secretes secrete, CCK, or GIP
–Paneth cells, secrete lysozyme and is capable of phagocytosis–immune cell
–located d on the apical membrane

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21
Q

describe bicarb secretion

A

due to the presence of acid inthe intestine, secretin is released into blood by the duodenum and binds to reeptors on the basolateral (blood side) membrane; scretin increases the activity of the Bicarb/Na transporter (2:1) –> bicarb builds up in cell, passively diffuses into lumen with the help of a chloride exchanger; as well, CO2 can passively diffuse through pancreas/intestinal cell and be converted to HCO3 + H+ via CA and then can pass through into lumen of pancreas or intestine

22
Q

describe bile acid reuptake

A

specific transporters in ileum which recognize conj. primary bile acids–ASBT (apical sodium-bile transporter) in ileum—go back to liver for re-secretion; not all primary acids go through, and are converted to secondary bile acids by bacteria in the colon—remove OH and deconjugate–taken up in colon
–enterohepatic circulation for secondary deconj?

23
Q

what are the functions of the gall bladder?

A

– Storage and concentration of bile (5-10x, from absorption of
water), receptive relaxation (NO-mediated)
– Bile from gallbladder aids digestion but is not essential for it, as liver keeps slow constant discharge of bile into duodenum

24
Q

describe the regulation of biliary secretions

A

– Fatty acids and proteins in the duodenum cause release of CCK (cholecystokinin)
– CCK increases gallbladder contraction, Acetylcholine also contracts and helps empty gallbladder
– Production of bile is increased by stimulation of the vagus nerves and by the hormone secretin

25
Q

describe how bile salts contribute to lipid digestion

A

presence of TAGs stim CCK release, causes gall to contract and release BS/BAs (in the form of micelles); it also acts on pancreatic acinar cells which causes the release of enzymes (e.g. pancreatic lipase) BA/BS emulsify large TAG droplets–>tiny droplets; now, PL can degrade them into MAGs and FAs; the BAs mix with the FAs/MAGs to create mixed micelles (also lipid sol vits A D E K)–>brings them to the unstirred layer of microvilli and dumps them off so they can diffuse through; once inside the cell, they reform TAGs which are then packaged into chylomicrons and exocytosed out of the BASAL membrane into lacteals; FAs can pass through basal membrane to capillary;

26
Q

what is the purpose of colipase?

A

-Bile salts prevent lipase digestion of fats,
but presence of colipase resumes fat digestion–it separates the bile acids on the fat droplet so lipase can access the TAGs in the middle to release MAGs and FAs
-Colipase not only facilitates digestion, it also facilitates transfer of lipid digestion products from fat drop into micelle

27
Q

describe the creation and secretion of chylomicron

A

secreted via epithelial cells –MAGs and FAs are re-esterified to form TAGs in the smooth ER; apolipo prots synth’d in the rough ER and glycosylated (via golgi)–> then coated around lipid core and secreted from BASOLATERAL POLE via exocyotisis;
• Chylomicrons, mainly triglyceride with phospholipids/apolipoproteins
• Contains small amount of cholesterol in center

28
Q

sources of blood for liver?

A 
hepatic PORTAL vein (75%)
hepatic artery (25%)
29
Q

what are hepatic sinusoids?

A

capillary bed in liver which mixes O2-rich blood from hepatic artery and nutrient rich blood from GI tract

30
Q

what is the hepatic portal triad?

A

where the bile duct, branch of hepatic portal vein, and branch of hepatic artery meet

31
Q

describe the types of cells found in a hepatic lobule

A

Stellate cells – stores vit A
Fenestrated endothelial cells, with “holes”
Hepatocytes, majority of cells –produce lots of enzymes for detoxing of drugs, modify hormones (prohormones—>hormones) secreted via endocrine cells of GI tract
Kupffer cells are phagocytic immune cells–phagocytose dead/dying RBCs, bacteria that has entered blood, etc

32
Q

what leaves the liver via the hepatic vein?

A 
Glucose
Plasma proteins 
Urea
Vit. D, 
Hormones
Metabolites for excretion
modified xenos
33
Q

what enters the liver via the hepatic artery?

A

Oxygen Nutrients Bilirubin Hormones Drugs

34
Q

what leaves the liver via bile?

A

Bile salts Bilirubin water, ions cholesterol, big xenos

35
Q

functions of the liver

A

(1) Production of bile
(2) Metabolic processing of absorbed nutrients
(3) Detoxification (drugs, hormones, foreign compounds)
(4) Synthesis of plasma proteins
(5) Storage (glycogen, fats, Fe, Cu, vitamins)
(6) Activation of vitamin D (along with the kidney)
(7) Removal of worn-out red cells (resident macrophages, Kupffer cells)
(8) Urea production

36
Q

describe the mucosal barrier to abs

A
  1. Unstirred layer of fluid
  2. Glycocalyx (“fuzzy coat”)
  3. Cell membrane
  4. Cytoplasm of enterocyte
  5. Basal or lateral cell membrane
  6. Intercellular space
  7. Basement membrane
  8. Membrane of capillary or lymph
37
Q

describe sugar digestion and uptake

A

starch is degraded by salivary/pancreatic amylases into short oligos, maltriose, or maltose; brush border enzymes in microvilli then further digest these sugars; e.g. sucrase (attached to isomaltase) breaks apart sucrose (fructose and glucose); glucose then goes into villi cell via SGLT-1, an Na-Glu cotransporter (also–improtant for absorption of water); galactose can also go through SGLT-1; fructose goes through GLUT5 passively;
lactase breaks apart glucose and galactase, again both being transported via SGLT-1 and Na.
–SGLT-1 is SECONDARY ACTIVE TRANSPORT
GLUT2 then transports all 3 monosacchs into capillary (apical membrane); also GLUT5 for fructose into cap

38
Q

describe protein assimilation

A

pancreatic enzymes released from exocrine cells, brush border enzymes, digestive juices, etc all lead to the formation of amino acid, di and tripeptides–enter into cells; amino acids enter through nonspecific or specific transporters; di and tri peptides enter through PEPT1 which also requires H+;
Dipeptides and tripeptides hydrolyzed into free amino acids in the cells later secreted into capillaries

39
Q

role of appendix

A

could store commensal bacteria in times of need; secrete into colon

40
Q

motility of the large intenstine?

A

– Haustral contractions
• non-propulsive, shuffle the colonic contents back and forth–mix food with bacteria, helps slow it down for more absorption and concentration of feces
• Similar to small intestine segmentation contractions but less frequent
– Mass movements, like peristaltic contractions
• Large segments of ascending and transverse colon contract simultaneously to move colonic contents further in the large intestine.
• 3-4x / day, after meals
–no specific hormones, not similar to MMC

41
Q

what is hirschprung’s disease?

A

no myenteric plx. ganglion–motility dysfunction – Severe constipation, 3-4 inch dilation of colon–leads to megacolon;

42
Q

describe the defacation reflex

A
  1. filling the rectum
  2. sense stretch in mechanoreceptors
  3. impulses to spinal cord
  4. contraction of rectum and relaxation of internal anal sphinc (sm muscle)
  5. voluntary relaxation of external anal sphinc (sk muscle)
  6. cord reflex adds intrinsic defecation reflex by MyP of colon wall
    A) Intrinsic defecation reflex (weaker) B) Parasympathetic def. reflex–can lose and still have normalish empttying
    (stronger, sacral or pelvic nerves)
43
Q

describe the types of colonocytes

A

NO VILLI,only crypts
absorptive cell with microvilli–absorbs water
goblet cell, secretes mucus
peyer’s patch–found in lamina propria, (also found in ileum) but mostly abundant in colon; houses immune cells (T cells, B cells, etc)

44
Q

This small adenomatous polyp (tubular adenoma) on a small stalk is seen microscopically to have more crowded, disorganized glands than the normal underlying colonic mucosa with fewer Goblet cells.
Get screened for colon cancer at age 50, if strong family history

A

ya

45
Q

large int secretion?

A

mucus from goblet cell for lubrication

46
Q

digestion of large int?

A

none except what is done by bacteria;
bacterial fermentation of dietary fibres
bacteria–proteins to amino acids, pigments (bilirubin to stercobilin)

47
Q

absorption in large int?

A

salt and water, some products of bacterial metabolism–B vits and vit K)

48
Q

Processes stimulated by insulin release

A

glycogenesis: glycogen formation in liver and muscle
lipogenesis: formation of fats for storage in mostly adipose tissue

49
Q

what are the direct and indirect actions of insulin?

A

indirect: stims fat storage, increases leptin secretion
direct: supresses NPY release in hypothal

50
Q

what are the actions of leptin?

A

is a satiety factor secreted by adipose tissue
Leptin crosses BBB and acts on arcuate nucleus of the hypothalamus, by decreasing release of NPY and agouti-related protein and stimulating release of MSH–>decreases appetite and increase metabolic rate

PHSI 208 (32 decks)

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